中国组织工程研究

中国组织工程研究 ›› 2010, Vol. 14 ›› Issue (20): 3611-3614.doi: 10.3969/j.issn.1673-8225.2010.20.001

• 软骨组织构建 cartilage tissue construction •    下一篇

肿瘤坏死因子α在肢体缺血再灌注损伤软骨中的表达

蒋 清1，胡懿郃2，魏利成1   

  1. 1邵阳市第一人民医院，湖南省邵阳市  422000；
    2中南大学湘雅医院骨科，湖南省长沙市  410008
  • 出版日期:2010-05-14 发布日期:2010-05-14
  • 通讯作者: 魏利成，硕士，副主任医师，邵阳市第一人民医院，湖南省邵阳市 422000 Weilicheng78@163.com
  • 作者简介:蒋 清，男， 1969年生，湖南省新邵县人，汉族，中南大学湘雅医学院在读硕士，副主任医师，主要从事骨组织工程研究。

Expression of tumor necrosis factor alpha in cartilage during limb ischemia-reperfusion injury

Jiang Qing1, Hu Yi-he2, Wei Li-cheng1   

  1. 1Shaoyang First People’s Hospital, Shaoyang  422000, Hunan Province, China;
    2Department of Orthopaedics, Xiangya Hospital, Central South University, Changsha  410000, Hunan Province, China
  • Online:2010-05-14 Published:2010-05-14
  • Contact: Wei Li-cheng, Master, Associate chief physician, Shaoyang First People’s Hospital, Shaoyang 422000, Hunan Province, China
  • About author:Jiang Qing, Studying for master’s degree, Associate chief physician, Shaoyang First People’s Hospital, Shaoyang 422000, Hunan Province, China Weilicheng78@163.com

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摘要：

背景：肢体缺血再灌注损伤的研究起步相对较晚，且主要集中在对肢体骨骼肌、神经等软组织的研究，对肢体缺血再灌注后关节软骨的损伤目前国内外却较少报道。

目的：观察肿瘤坏死因子α在肢体缺血再灌注损伤时不同时间段内软骨中的表达变化。

方法：将SD大鼠随机分为假手术组、缺血6 h组、缺血6 h再灌注1，3，7，14，30，60 d组。建立大鼠肢体缺血再灌注损伤模型。分别于缺血再灌注后相应时间点处死动物，切取左胫骨平台内侧软骨组织做苏木精-伊红染色观察软骨的组织形态学变化，免疫组织化学检测软骨中肿瘤坏死因子α表达水平的变化。

结果与结论：早期(7 d内)软骨组织学光镜下改变不明显；后期损伤加重，可见软骨变薄，排列紊乱，表面不完整，偶见软骨缺损。假手术组肿瘤坏死因子α阳性表达较弱，缺血6 h组阳性表达开始增强，再灌3，7 d组达到高峰，随后阳性表达下降；再灌60 d组与假手术组相比差异仍有显著意义(P < 0.05)。结果表明，肢体缺血再灌注可导致关节软骨的损伤。肢体缺血再灌注损伤时，关节软骨中肿瘤坏死因子α增加在软骨损伤中发挥重要作用。

关键词: 缺血再灌注, 肢体软骨损伤, 肿瘤坏死因子&alpha, 软骨组织工程, 大鼠

Abstract:

BACKGROUND: Studies of limb ischemia-reperfusion (IR) injury was developed relatively later, and most of these focused on soft tissues such as skeletal muscle and nerves. The damage of articular cartilage during limb IR injury is rarely reported both in China and abroad.

OBJECTIVE: To investigate the expression of tumor necrosis factor α (TNF-α) in articular cartilage at different time points of limbs IR injury.

METHODS: SD rats were randomly divided into the sham-operated, ischemia 6 h, and IR groups (1, 3, 7, 14, 30, and 60 d). Rats were established for limb IR models. The grouped rats were killed at each time point, respectively. The articular cartilages were excised from the medial of the left keen joints. The pathological changes of articular cartilage were observed by hematoxylin-eosin staining, and the expression of TNF-α was detected by immunohistochemistry. 

RESULTS AND CONCLUSION: Under light microscope, cartilage cells lightly swelled at 7 days after reperfusion and got worse with time prolonged. In the sham-operated group, positive TNF-α was weak expressed and increased in the ischemia 6 h group, peaked in the IR 3 d, 7 d groups and then began to decrease. There were significant differences between the IR 60 d group and the sham-operated group (P < 0.05). All results demonstrated that limb IR injury could cause the injury of articular cartilage. Increasing TNF-α played an important role in the articular cartilage after limb IR injury.

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